Karolinska Institutet
Department of Neurobiology, Care Sciences and Society
I hold a medical degree from the University of Ioannina and a Master’s degree in neuroscience from the University of Crete, within the interdisciplinary graduate programme ‘Brain & Mind’. During my MSc studies, I gained broad experience in the field of both molecular and computational neuroscience. My assignments have focused on neuropharmacology, physiology experiments involving non-human primates (NHPs) and neurophysiological data analysis. Currently, as a member of Prof. Nordberg's Translational Molecular Imaging Lab, I aspire to expand my knowledge on molecular neuroimaging and neurodegenerative diseases biomarkers. In particular, I hold a special interest in the understanding of pathophysiological mechanisms of tauopathies, such as Alzheimer’s disease (AD), with the use of Positron Emission Tomography (PET) tracers, plasma and Cerebrospinal Fluid (CSF) biomarkers. My goal is to combine the above methods with the clinical examination for the early diagnosis of AD and contribute to the development of disease-modifying treatments.

Presenter of 1 Presentation

HIGH TAU LOAD IS COUPLED WITH BOTH AMYLOID-BETA PATHOLOGY AND FAST FUTURE COGNITIVE DECLINE

Session Type
SYMPOSIUM
Date
Sat, 19.03.2022
Session Time
05:15 PM - 07:15 PM
Room
ONSITE: 114
Lecture Time
05:30 PM - 05:45 PM

Abstract

Aims

Amyloid-beta Positron Emission Tomography (PET) efficiently detects Alzheimer’s disease (AD) pathology in cognitive impaired patients, but lacks specificity regarding the prediction of future cognitive status. The increasing validation of tau PET tracers raises questions about whether this biomarker could predict clinically relevant cognitive decline in the AD continuum.

Methods

We selected 293 subjects [cognitive normal (CN; n=196), mild cognitive impairment (MCI; n=80), dementia (n=17)] with baseline amyloid-beta and tau PET scans that have completed a follow-up of at least two years, from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) dataset. Based on Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAS-Cog) and linear mixed-effects models, all individuals were clustered as either fast or slow decliners. Group comparisons and accuracy of discrimination were tested.

Results

The individuals with amyloid-beta positivity and fast cognitive decline showed the highest tau PET binding values independently of baseline cognitive status, compared to the other groups (amyloid-beta negative with fast or slow decline and amyloid-beta positive with slow decline). Baseline tau PET binding could determine fast decliners with a amyloid-beta positive scan with an accuracy of 87% (composite temporal region of interest). Tau PET showed a similarly high accuracy to determine patients with MCI that would be both amyloid-beta positive and show a progress in their diagnosis at follow-up.

Conclusions

High baseline tau load is coupled with both amyloid-beta pathology and an accelerated profile of cognitive decline. Tau PET usage could offer substantial advantages over amyloid-beta PET since it gives information about the underlying pathophysiology and prognosis of the disease.

adpd2022figure.jpg

Hide